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Cardiovascular System > Session 2 > Flashcards

Session 2 Flashcards

1
Q

Why do we need a cardiovascular system?

A
  • Getting the oxygens and nutrients close to the cells as the diffusion distance is too big for simple diffusion.
  • Removal of waste and carbon dioxide from the blood and into lungs to be removed.
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2
Q

What are capillaries?

A

Composed of a single layer of endothelial cells surrounded by basal lamina. Also have gaps between endothelial cells to allow small water soluble molecules to enter.

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3
Q

Why does the heart need its own blood supply?

A
  • LV is filled with oxygenated blood but it’s too thick for the oxygen to diffuse
  • Has a blood supply of coronary arteries.
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4
Q

What are the main coronary arteries? (LABEL ON DIAGRAM)

A
  • Left anterior descending artery
  • Circumflex artery
  • Left main artery
  • Right coronary artery
  • Right marginal artery
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5
Q

What are the problems with coronary arteries?

A
  • End arteries: do not anastomose so connections are not made
  • Prone to atheromas and possibly eventual blockages and therefore MIs.
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6
Q

What are the layers of the pericardium?

A
  • Endocardium
    Protection to valves and heart chambers
  • Myocardium
    Cardiac muscle
  • Visceral layer
    Inner serous layer that secretes small amounts of fluid
  • Parietal layer
    Outer serous layer
  • Fibrous layer
    Anchors heart to the surrounding walls and prevents overfilling
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7
Q

What are the pressures in systemic and pulmonary circulations?

A

S: 120/80 (high)
P: 25/10 (low)

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8
Q

What is coordinated contraction?

A

Both sides of the heart contract at the same time and pump the same volume of blood to maintain stroke volume.

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9
Q

What is systole?

A

Contraction and ejection of blood from ventricles

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10
Q

What is diastole?

A

Relaxation and filling of ventricles

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11
Q

How much blood does the heart pump per minute at a heart rate of 70 bpm?

A

4.9 L/min (approx. volume of blood in a 70kg average man)

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12
Q

What is the heart muscle?

A
  • Specialised form of muscle
  • Have gap junctions for communications (intercalated discs)
  • Contract in response to an action potential triggered by spread of an excitation wave from cell to cell
  • Action potential lasts for the whole duration of a whole contraction, aka. 280 ms.
  • Figure of 8 arrangement
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13
Q

What are the four heart valves?

A
  • Mitral valve (right side, blood in)
  • Tricuspid valve (left side, blood in)
  • Pulmonary valve (right side, blood out)
  • Aortic valve (left side, blood out)
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14
Q

How do valves work?

A
  • Open/close depending on the pressure difference
  • Valve cusps open to allow blood to flow in and close to seal and prevent blood back flow
  • Cusps of mitral + tricuspid connected to PAPILLARY MUSCLE AND CHORDAE TENDINAE to prevent inversion of valves
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15
Q

When are valves open?

A

Mitral + tricuspid open = aortic and pulmonary closed and vice versa

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16
Q

What is the cardiac conduction system?

A
  • Action potential generated by pacemaker cells in the SAN
  • Activity spreads over atria = atrial systole
  • Wave reaches AVN and pauses for 120ms to allow atria to finish contraction
  • Excitation from AVN spreads down septum
  • Spreads to ventricular myocardium from endocardial to epicardial surface
  • Ventricular contraction from the apex up
  • Blood forced through outflow valves
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17
Q

What is the Wiggers diagram?

A

A diagram showing all the changes in volume and pressure during cardiac contraction

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18
Q

What is atrial contraction?

A

Phase 1.

  • Atrial pressure rises (A wave)
  • P wave in ECG - atrial depolarisation
  • Atrial contraction = 10% of ventricular filling (90% passive)
  • Mitral/tricuspid valves open
  • Ventricles reach EDV = 120ml
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19
Q

What is isovolumetric contraction?

A

Phase 2.

  • Mitral valve closure: IV pressure > Atrial pressure
  • Ventricle contracts: rise in pressure
  • C wave due to mitral valve closure
  • No change in ventricular volume as all valves closed and blood can’t move
  • QRS - ventricular depolarisation
  • Closure of valves = S1 (FIRST HEART SOUND)
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20
Q

What is rapid ejection?

A

Phase 3.

  • IV pressure > Aortic pressure: aortic valve opens
  • Atrial base pulled downward as ventricle contracts (X-DESCENT)
  • Rapid drop in ventricular volume = blood into aorta
  • Mitral + tricuspid valves closed
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21
Q

What is reduced ejection?

A

Phase 4.

  • Decline in ventricular pressure, rate of ejection falls
  • Atrial pressure rises due to venous return from lungs (V wave)
  • Ventricular depolarisation - T wave
  • Aortic/pulmonary valves open
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22
Q

What is isovolumetric relaxation?

A

Phase 5.

  • Aortic pressure > IV pressure = back flow of blood, makes aortic valve close
  • Valve closure = dicrotic notch
  • Decline in ventricular pressure but volume constant as all valves closed
  • END SYSTOLIC VOLUME (70-80ml)
    (EDV - ESV = stroke volume)
  • Closure of aortic/pulmonary valves - S2 heart sound
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23
Q

What is rapid filling?

A

Phase 6.

  • Fall in atrial pressure after mitral valve opens = Y descent
  • Atrial pressure > IV pressure = mitral valve opening, ventricular filling begins
  • Normally silent but sometimes S3 sound present - normal in children, may be pathology in adults
  • Mitral/tricuspid valves open
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24
Q

What is reduced filling?

A

Phase 7.

  • Diastasis: rate of filling slows down
  • Ventricle reaches inherent relaxed volume
  • More filling due to venous pressure
  • 90% full ventricles, extra 10% from atrial contraction
  • Mitral/tricuspid valves open
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25
Q

What is valve regurgitation?

A

Valve doesn’t close all the way and there is back leakage of blood into ventricle

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26
Q

What is valve stenosis?

A

Valve doesn’t open enough and there is obstruction to blood flow

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27
Q

What is aortic valve stenosis?

A
  • Less blood gets through = increased LV pressure and LV hypertrophy
  • Left sided heart failure; not enough blood around body = angina and syncope
  • Stress = microangiopathic haemolytic anaemia as blood cells burst
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28
Q

What are causes of aortic valve stenosis?

A
  • Degeneration (senile fibrosis/calcification)
  • Congenital (bicuspid when normally tricuspid)
  • Chronic rheumatic fever - commissural fusion (autoantibodies attack valve)
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29
Q

What kind of murmur does aortic valve stenosis create?

A

Crescendo-decrescendo systolic murmur

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30
Q

What are the causes of aortic valve regurgitation?

A
  • Valvular damage (eg. endocarditis)

- Aortic root dilation - leaflets pulled apart

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31
Q

What is aortic valve regurgitation?

A
  • Blood flows back into LV
  • Stroke volume increases
  • Systolic pressure increases
  • Bounding pulse, head bobs and nails flush with piles
  • LV hypertrophy
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32
Q

What is mitral valve regurgitation?

A
  • Chordae tendinae & papillary muscles stop preventing prolapse = Prolapse
  • Increased preload = LV hypertrophy
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33
Q

What kind of murmur does aortic valve regurgitation create?

A

Diastolic murmur (after S2)

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34
Q

What are the causes of mitral valve regurgitation?

A
  • Damage to papillary muscle (MI)
  • Left sided heart failure (LV stretch)
  • Rheumatic fever (leaflet fibrosis)
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35
Q

What kind of murmur does mitral valve regurgitation create?

A

Holosystolic murmur (after S2, short)

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36
Q

What is mitral valve stenosis?

A
  • Commissural fusion of valve leaflets
  • Caused by rheumatic fever mostly
  • Blood struggles to flow from LA to LV = increased LA pressure
  • LA dilation can cause: AF, thrombus formation, oesophagus compression (+ dysphagia)
  • Pulmonary oedema + hypertension, RV hypertrophy
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37
Q

What kind of murmur does mitral valve stenosis create?

A
  • Snap as valve opens

= Diastolic rumble

38
Q

What is the afterload?

A

The load that the heart must eject blood against (equivalent to aortic pressure)

39
Q

What is the preload?

A

Amount the ventricles are stretched in diastole (EDV/central venous pressure)

40
Q

What is total peripheral resistance?

A

Resistance to blood flow offered by all the systemic vasculature

(More constricted vessels = higher peripheral resistance)

41
Q

Why do arterioles offer the greatest resistance?*

A
  • More smooth muscle in tunica media
  • Narrows lumen
  • Reduces pressure before capillaries so capillaries do not burst
42
Q

What happens when the vessels are constricted?*

A
  • Resistance causes a pressure drop
  • Will drop on venous side
  • Will rise on arterial side
43
Q

What happens if you decrease TPR?* (and CO is unchanged)

A
  • Arterial pressure falls (easier pumping)

- Venous pressure rises (more blood reaches veins)

44
Q

What happens if you increase TPR?* (and CO is unchanged)

A
  • Arterial pressure increases (higher pressure needed to pump blood through the resistance)
  • Venous pressure decreases (less blood getting through)
45
Q

What happens if CO increases and TPR stays the same?*

A
  • Arterial pressure increases (heart pumping out more blood)
  • Venous pressure decreases (heart is being emptied more)
46
Q

What happens if CO decreases and TPR stays the same?*

A
  • Arterial pressure decreases (less blood pumped around body)
  • Venous pressure increases (heart not emptied as much)
47
Q

Why can heart failure occur with increased venous pressure when CO decreases?

A
  • Blood does not leave the heart quickly enough
  • Heart is not emptied as much so SV is increased

PULMONARY/PERIPHERAL OEDEMA

48
Q

What happens when the heart needs more blood?

A

Arterioles and precapillary sphincters dilate so TPR falls and the heart can pump more blood so that there are no changes in pressure

49
Q

How does the heart respond to changes in central venous pressure and arterial blood pressure?

A

Extrinsic and intrinsic mechanisms.

50
Q

What is the meaning of afterload?

A

Load that the heart must eject blood against (eg. aortic pressure; higher pressure = higher load)

51
Q

What is the meaning of preload?

A

The amount that the ventricles are stretched/filled in diastole (EDV/CVP)

52
Q

What is the meaning of total peripheral resistance?

A

Resistance to blood flow offered by all systemic vasculature (more constricted vessels = higher peripheral resistance)

53
Q

Why do arterioles offer the greatest resistance?

A
  • Narrow lumen

- Have more smooth muscle in tunica media

54
Q

What happens when arterioles constrict?*

A
  • Increased resistance
  • Pressure in capillaries on venous side falls (constriction causes drop in pressure)
  • Pressure on arterial side rises

MORE RESISTANCE = LARGER PRESSURE DROP

55
Q

What happens when TPR falls and CO is unchanged?*

A
  • Arterial pressure falls

- Lower resistance means increased venous pressure as more blood reaches the veins more readily

56
Q

What happens when TPR is increased and CO is unchanged?*

A
  • Arterial pressure increases as it’s harder to pump blood through the constriction
  • Venous pressure falls as blood is not getting through as easily
57
Q

What happens when CO increases and TPR stays the same?*

A
  • Arterial pressure increases as heart is pumping out more blood
  • Venous pressure reduces as heart is emptied out more
58
Q

What happens when CO decreases and TPR stays the same?*

A
  • Arterial pressure drops as less blood is pumped around body
  • Venous pressure rises as heart is not emptied out as much and heart failure can occur, as well as pulmonary and peripheral oedema
59
Q

What happens when tissues need more blood?

A
  • Arterioles and precapillary sphincters dilate

- Peripheral resistance falls, so heart pumps more blood to prevent drop in arterial blood pressure caused by lower TPR

60
Q

How does the heart respond to changes in certain venous pressure and arterial blood pressure?

A
  • Intrinsic mechanisms: myocardial cells

- Extrinsic mechanisms: neural/hormonal effects

61
Q

How do you calculate cardiac output?*

A

Heart rate x stroke volume

62
Q

How do you calculate stroke volume?

A

End diastolic volume - end systolic volume

63
Q

How can stroke volume be increased?

A
  • Increasing end diastolic volume

- Decreasing end systolic volume

64
Q

When does ventricular filling occur?

A

Diastole

65
Q

How does the ventricle fill and how is it dependent on pressure?*

A
  • Ventricle fills until walls stretched enough to produce pressure in ventricles equal to venous pressure
  • Higher venous pressure = more filling of heart
  • More filling = higher LV pressure
66
Q

What is decreased compliance?

A
  • Stiff heart (less filling)
  • Hypertrophy
  • Higher pressure
67
Q

What is increased compliance?

A
  • Heart dilated (more filling)

- Lower pressure

68
Q

What is the Frank-Starling law of the heart?

A
  • INTRINSIC CONTROL MECHANISM
  • The more the heart fills, the harder it contracts (up to a limit)
  • Harder heart contracts = bigger stroke volume
  • Increase in venous pressure fills heart more
69
Q

What influences how much ventricles fill?

A

Compliance (eg. stiffness/dilation)

70
Q

What is the Starling curve and what does it show?*

A
  • Increased venous return = increased left ventricular end-diastolic pressure and preload
  • Increase in SV
71
Q

What is the length-tension curve for cardiac muscle and why is it relevant?*

A

Shows that the length of the sarcomere matters.

  • Too short: filament overlap interferes w/ contraction
  • Stretching of muscle causes increase in Ca2+ sensitivity and increases the force of contraction
72
Q

What is the purpose of the Frank-Starling law of the heart?*

A
  • Ensuring that both sides of the heart maintain the same output
  • Allows pulmonary and systemic circulation to operate in series
  • Same volume of blood pumped to the body and lungs
73
Q

What is contractility?

A

Force of contraction for a given fibre length (how hard the fibre will contract)

74
Q

What does a change in contractility cause?*

A
  • Change in slope of Starling curve

- Increase = increased force of contraction

75
Q

What can affect contractility?

A 
Increase = sympathetic stimulation, circulating adrenaline
Decrease = reducing sympathetic stimulation
76
Q

When does aortic pressure increase?

A

When peripheral resistance increases, which makes it harder for the heart to pump

77
Q

Why does increased TPR reduce filling of the heart?

A

Reduces venous pressure

78
Q

What determines cardiac output (how much the ventricle empties)?

A
  • Force of contractions (EDV and contractility)
  • How hard it is to eject blood (aortic impedance)
  • Cardiac output
79
Q

What controls contractility and heart rate?

A

Autonomic nervous system

80
Q

What will a decrease in arterial BP cause?

A
  • Reduce parasympathetic NS activity
  • Stimulates sympathetic NS activity

= Increases HR and contractility

81
Q

What happens if the body metabolism increases?

A
  • TPR will reduce due to dilating arterioles
  • Fall in arterial pressure
  • Rise in venous pressure
  • Heart responds by pumping more
82
Q

How does the CVS respond to eating a meal?*

A
  • Local vasodilation in gut

Slide 23! :) Notes!

83
Q

What happens when you stand up?

A
  • Gravity action causes blood to pool in legs

- Venous pressure decreases, and so does CO and arterial pressure

84
Q

What increases HR and TPR?

A
  • Baroreceptor reflex

- Autonomic NS

85
Q

What happens if reflexes don’t work?

A

Postural hypotension

86
Q

What happens during exercise?*

A
  • Muscle pumping and venoconstriction return more blood to heart
  • TPR decreases - increased venous return
  • Increased heart rate and contractility (sympathetic drive)
87
Q

How is a jugular venous pulse measured and what is it?

A
  • Biphasic pulse: two peaks per cardiac cycle, one weak and one small (‘beats’ twice)
88
Q

Where can the JVP be felt?

A

Behind the sternocleidomastoid muscle

  • Normally 5-8cm H2O
  • Can be measured with a central line inserted into internal jugular vein to allow seeing waveform
89
Q

How does height of JVP vary over time?* (DIAGRAM)

A
  • Atrial systole (rise)
  • Atrial diastole (fall)
  • Tricuspid valve closure (rise)
  • Ventricular systole (fall)
  • Maximum atrial filling pressure (rise)
90
Q

What causes JVP pressure to rise?

A
  • Right sided heart failure
  • Volume overload (IV infusion)
  • Impaired filling of heart
  • e.g. stab wounds

Cardiovascular System (11 decks)

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